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At least 19 recordsLinked to original sources

PubMed1992

Tracer studies of urea kinetics in growing pigs: I. The effect of intravenous infusion of urea on urea recycling and the site of urea secretion into the gastrointestinal tract.

Four gilts (average BW 80 kg) were used in the first experiment to study the effect of i.v. infusion of urea on urea kinetics by means of a radioisotope dilution technique. The pigs were fed twice daily 600 g of a cornstarch-based diet formulated to contain 16% CP by supplementation with isolated soy protein. Infusion of urea, compared with saline, increased (P < .05) plasma urea concentration, urea pool size, urea entry, urea excretion, and urea degradation rates; urea turnover rate and urea space were not affected (P > .05). Expressed as a percentage of the total entry rate, a lower (P < .05) percentage of urea was recycled in pigs infused with urea. The urea infused was almost completely excreted in urine, so there were no differences (P > .05) in N balance. In the second experiment, four gilts (average BW 40 kg), fitted with ileocecal reentrant cannulas, were used to determine whether the upper or the lower digestive tract represents the preferential site of urea secretion in pigs. Two pigs were fed twice daily 600 g of a cornstarch-based diet, formulated to contain 16% CP from soybean meal. The other two pigs were fed the same diet in which 15% cornstarch was replaced by beet pulp. After labeling the body urea pool of one pig on each treatment with [15N]urea, the reentrant cannulas were disconnected to prevent the flow of digesta from the small into the large intestine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

GC-MS determination of ratios of stable-isotope labelled to natural urea using [13C15N2]urea for studying urea kinetics in serum and as a means to validate routine methods for the quantitative assay of urea in dialysate.

A GC-MS determination of urea in serum or spent dialysate is described, using 13C15N2-labelled urea and assaying the area ratio of labelled to natural urea by mass fragmentographic monitoring of fragments m/e 153 and 156, after its eventual conversion into the trimethylsilylether-derivative of 2-hydroxypyrimidine. The procedure can be successfully applied in the follow-up of the disappearance of labelled urea in serum after intravenous injection in man, enabling kinetic parameters of urea to be established, e.g. for purposes of studying the effectiveness of dialysis procedures. Furthermore the method can be used for validation of routine methods for measuring urea in other fluids, in particular dialysate. Examples are given of both applications of the GC-MS method described.

Calibration↗

PubMed1982

Urea handling by the distal tubule and collecting duct of the rat during urea--saline, isotonic saline, or urea diuresis.

The aims of the present study were to examine the effects of urea and isotonic saline loads separately and together on urea handling in the medullary collecting duct and surface distal tubules of the rat kidney. Microcatheterization of the medullary collecting duct during isotonic saline diuresis (saline at 5% of body weight per hour, plasma urea 4.3 mM/L), showed an increase in the remaining fraction of filtered urea from 56.2% at the beginning (corticomedullary junction) to 68.5% at the end (papillary tip) of the medullary collecting duct (n = 17 paired samples in six rats, p less than 0.05). There was no change in the fraction of filtered urea along the medullary collecting duct during urea diuresis (plasma urea 87 mM/L, n = 15 paired samples in six rats) or during urea--saline diuresis (plasma urea 103 mM/L, n =32 paired samples in nine rats). Micropuncture of surface distal tubules in the same animals showed an increase in the fraction of filtered urea between end-distal samples and the beginning of the medullary collecting duct from 28.9 to 56.2% during isotonic saline diuresis (p less than 0.001), and from 53.6 to 75.3% during urea--saline diuresis (p less than 0.01), but no change during urea diuresis (63.6 to 60.0%, p = NS). Our conclusions are as follows. (1) Urea entry into the medullary collecting duct during steady-state diuresis occurs at low intratubular urea contractions (isotonic saline diuresis) but not at high concentrations (urea--saline diuresis and urea diuresis). (2) Urea entry between the surface distal tubule and the beginning of the medullary collecting duct occurs during saline diuresis (isotonic saline diuresis and urea--saline diuresis) but not urea diuresis. The latter finding suggests that isotonic saline loads affect urea transport differently in juxtamedullary nephrons compared to superficial nephrons.

Animals↗

PubMedDate not supplied

Liquid chromatographic determination of urea in water-soluble urea-formaldehyde fertilizer products and in aqueous urea solutions: collaborative study.

Water soluble urea-formaldehyde (UF) fertilizers, manufactured by complex reaction of urea and formaldehyde, typically contain varying amounts of unreacted urea. A liquid chromatography method for the analysis of urea in these products, and in aqueous urea solutions, was collaboratively studied. An amine chromatography column was used to separate the unreacted urea from numerous UF reaction products present in these liquid fertilizers. Unreacted urea was determined by using external urea standards with UV detection at 195 nm. The standards and test samples were prepared in the mobile phase of 85% (v/v) acetonitrile in water. Ten laboratories analyzed 5 different UF-based commercial products containing unreacted urea in the range of 6 to 17% by weight, and 5 different concentrations of urea in water equivalent to commercial products of that nature. The aqueous urea solutions contained 2-20% urea (w/w). The range of s(R) values for the 5 UF-based commercial fertilizers was 0.49-1.02 and the %RSD(R) was 1.94-6.14. The s(R) range for the 5 urea solutions was 0.10 to 0.79 and the %RSD(R) range was 2.54 to 4.88. The average recovery of urea from the aqueous urea solutions was 96-103%. Therefore, this method is capable of monitoring urea nitrogen manufacturers' label claims and total nitrogen claims in those cases where urea is the sole source of plant food nitrogen. Based on the collaborative study data, the authors recommend this method be approved for AOAC Official First Action status.

Chromatography, Liquid↗

PubMed1998

Estimation of urea production rate with [15N2]urea and [13C]urea to measure catabolic rates in diabetes mellitus.

For verifying catabolic states in insulin-dependent patients and dogs the method estimating urea production rates with 13C and with doubly 15N labeled urea, respectively, has been established. For a fast steady state of urea tracer dilution, a prime of 600 times the continuous infusion rate had to be injected. Urea was isolated from plasma samples by protein precipitation and cation exchange chromatography with a consecutive derivatization of the dried urea fraction (trimethylsilyl derivatives). The masses of the fragment ions m/z 189 (14N14N), 190 (14N15N) and 191 (15N15N) urea are monitored to estimate the [15N2] urea frequency in the overall body urea pool in mol percent excess (MPE). 1 to 15 ng of derivatized urea were measured efficiently. An excellent correlation between expected standard and measured MPE (r = 0.9977) was achieved from solutions containing 1 to 7% [15N2]urea. The interassay coefficient of variation amounted to < 10% for a [15N2]urea portion of > or = 3%. Normoglycemic diabetic patients who were treated with insulin overnight showed significantly higher urea production compared to healthy controls (9.22 +/- 2.07 vs. 5.4 +/- 0.32 mumol.kg-1.min-1; p < 0.05). Measurements in chronic diabetic dogs proved an increased rate of amino acid catabolism (+20% urea production) in systemic versus portal application of insulin in paired studies. This increased nitrogen load in diabetics may accelerate progression of diabetic nephropathy. Thus, the established stable isotope technique may serve as a sensitive and useful indicator of amino acid catabolism in clinical and experimental research.

Animals↗

PubMedDate not supplied

Salivary concentrations of urea released from a chewing gum containing urea and how these affect the urea content of gel-stabilized plaques and their pH after exposure to sucrose.

The objectives were to: (1) determine the salivary concentrations of urea during 20 min chewing of a sugar-free gum containing 30 mg of urea; (2) measure the degree to which this urea would diffuse into a gel-stabilized plaque; (3) study the effect of the urea on the fall and subsequent rise in pH (Stephan curve) on exposure to 10% sucrose for 1 min; (4) model the measurements 2 and 3 mathematically. In point 1, the salivary urea concentration of the 12 subjects peaked at 47 mmol/l in the first 2 min of gum chewing, falling within 15 min to the unstimulated salivary concentration of 3.4 mmol/l. Recovery of urea from the saliva averaged 81.5%. 'Plaques' of 1% agarose or 67% dead bacteria in agarose accumulated urea from the saliva roughly as expected, whereas those plaques containing 8% live and 59% dead Streptococcus vestibularis showed negligible accumulation. Computer modelling showed this difference to be due to urease of live bacteria breaking down the urea as rapidly as it entered the plaque. Simulation of the effect of gum chewing subsequent to initiation of a Stephan curve in the latter type of plaque showed a rapid rise in pH but then a fall again on return to unstimulated conditions. This fall had not been seen in previous studies, with Streptococcus oralis, nor was it predicted by the computer modelling. Neither experimental simulation nor computer modelling suggested that chewing urea-containing gum before exposure to sucrose would have any effect on a subsequent Stephan curve. Thus chewing gum is only likely to inhibit caries when it is chewed after consumption of fermentable carbohydrate, rather than before.

Adult↗

PubMed1986

Studies on the secretion of amino acids and of urea into the gastrointestinal tract of pigs. 3. Secretion of urea determined by continuous intravenous infusion of 15N-urea.

Three pigs, of 34 kg live weight, were each fitted with re-entrant cannulas both in the duodenum and terminal ileum and catheters in the jugular vein and in the carotid artery. Pigs received a diet based on wheat and dried skimmed milk in equal amounts at 12 h intervals. During the preliminary period the digesta flowing from both duodenal and ileal cannulas were collected over 12 h after feeding on two consecutive days and half of them were reintroduced into the gut and half were stored at -20 degrees C. During the experimental period 15N-urea was infused into the jugular vein for 12 hours starting with the morning meal. Total amount of urea infused was 5 g containing 1.22 g 15N-excess. The digesta from both proximal duodenal and ileal cannulas were collected and stored, while the digesta from the preliminary period were reintroduced into the respective distal cannulas. Blood samples were taken at different time of infusion. At the end of infusion period the animals were sacrificed and samples of the contents of the digestive tract and tissues were taken. Urea flux calculated according to atom-% 15N-excess of urea N in plasma was 1.23 to 2.37 g/kg body weight/day. In the duodenal digesta 94.5 +/- 0.2 and in ileal digesta 57.1 +/- 7.39 per cent of 15N were in the TCA soluble fraction. The total amount of 15N in the duodenal digesta was 1.7 to 6.3 times greater than in the ileal digesta. Only small amount of 15N was found in the caecum and almost none in the contents of colon and rectum. It is concluded that urea is secreted into all parts of the digestive tract, the main sites of urea secretion being pancreatic juice and/or bile as well as the small intestine. The total amount of urea secreted is assumed to be similar to the daily urea excretion.

Amino Acids↗

PubMed2001

Mechanisms of urea tolerance in urea-adapted populations of Drosophila melanogaster.

When behavioral avoidance cannot prevent an animal from being exposed to novel environmental toxins, physiological mechanisms must cope with the toxin and its effects. We are investigating the basis of urea tolerance in populations of Drosophila melanogaster that have been selected to survive and develop in food containing 300 mmol l(-1) urea. Previous research has demonstrated that the urea-selected larvae have lower levels of urea in their body than control larvae reared under the same conditions. The current series of experiments focuses on three possible ways of reducing urea levels in the body: urea metabolism, increased urea excretion and decreased urea uptake from the environment. We tested for urea metabolism directly, by assaying for activity of two urea-metabolizing enzymes, and indirectly, by looking for reduced urea content of their medium. To measure urea excretion rates in whole animals, we reared control and urea-selected larvae on urea-containing food (urea food), switched them to normal food and monitored the loss of urea from their hemolymph. We measured urea uptake by rearing control and selected larvae on normal food, switching them to urea food and monitoring the rate of urea appearance in the hemolymph. We found no evidence for urea metabolism by either direct or indirect methods. Control larvae excreted urea at a higher rate than selected, probably because they contained more urea than the selected larvae and thus had a greater gradient for urea loss. The rate of urea uptake in selected larvae was 2 mmol l(-1) h(-1) slower than the rate in control larvae, a difference that could account for the measured differences in body urea levels. Thus the selected larvae appear to have adapted to urea exposure primarily by decreasing the ability of urea to enter their body in the first place. The mechanism responsible for this reduction in uptake is uncertain.

Adaptation, Physiological↗

PubMedDate not supplied

[Blood urea concentration, a parameter for the assessment of protein metabolism in pregnant sows. 2. Relations between blood urea concentration and urine nitrogen excretion as well as estimation of urine nitrogen excretion from the blood urea concentration].

The influence of supplementing the ration with the limiting amino acid lysine on N-excretion in urine and the urea concentration in the blood (UCB) is investigated in an experiment with pregnant young sows. In contrast or the basic ration the most satisfactory N-utilisation reflects itself after a lysine intake of 8.2 g/animal and day during the early phase of gestation and 8.6 g during the last phase of gestation both in a diminished N-excretion in urine and a lower UCB. The following correlation coefficients were calculated for the relation between UCB an N-excretion in urine: early phase of gestation: 0.177 (n = 37); last phase of gestation. 0.431 (n = 30); gestation as a whole: 0.416 (n = 67). In a second experiment methionine supplementation in the feeding of a ration with a deficit of sulphur-containing amino acids led to a significant decrease of N-excretion in urine (alpha = 5%). While UCB also significantly decreased 5 hours after feeding, UCB virtually did not react to a changed level of amino acid intake when the blood sample was taken before feeding. In a third experiment, in which 49 g N/animal and day were taken in, differences regarding N-excretion in urine and UCB between pregnant and non-pregnant animals could not be established. When the results published in the first communication (Herrmann and Schneider, 1981) are included, the following correlation coefficients for the relation between N-excretion in urine and UCB are the result: 0.716 (n = 182) for sampling before feeding and 0.808 (n = 133) for sampling 5 hours after feeding. The confidence range of the estimated function y = -2.97 + 1.233 chi for the relation between N-excretion in urine (y; g/animal and day) and UCB 5 hours after feeding (chi; mg/100 ml serum) as well as the variability values do not make it possible to estimate N-excretion in urine from UCB with satisfactory accuracy.

Animals↗

PubMed1997

Determination of urea kinetics by isotope dilution with [13C]urea and gas chromatography-isotope ratio mass spectrometry (GC-IRMS) analysis.

1. Stable urea isotopes can be used to study urea kinetics in humans. The use of stable urea isotopes for studying urea kinetic parameters in humans on a large scale is hampered by the high costs of the labelled material. We devised a urea dilution for measurement of the distribution volume, production rate and clearance of urea in healthy subjects and renal failure patients using the inexpensive single labelled [13C]urea isotope with subsequent analysis by headspace chromatography-isotope ratio MS (GC-IRMS) of the [13C]urea enrichment. 2. The method involves measurement of the molar percentage excess of [13C]urea in plasma samples taken over a 4 h period after an intravenous bolus injection of [13C]urea. During the sample processing procedure, the plasma samples together with calibration samples containing a known molar percentage excess of [13C]urea are acidified with phosphoric acid to remove endogenous CO2, and are subsequently incubated with urease to convert the urea present in the plasma samples into CO2. The 13C enrichment of the generated CO2 is analysed by means of GC-IRMS. This method allows measurement of the molar percentage excess of [13C]urea to an accuracy of 0.02%. 3. Reproducibility studies showed that the sample processing procedure [within-run coefficient of variation (CV) < 2.8% and between-run CV < 8.8%] and the GC-IRMS analysis (within-day CV < 1.3% and between-day CV < 1.3%) could be repeated with good reproducibility. 4. In clinical urea kinetic studies in a healthy subject and in a renal failure patient without residual renal function, reproducible values of the distribution volume, production rate and clearance of urea were determined using minimal amounts of [13C]urea (25-50 mg). 5. Because only low [13C]urea enrichments are needed in this urea dilution method using GC-IRMS analysis, the costs of urea kinetic studies are reduced considerably, especially in patients with renal failure.

Adult↗

PubMed1993

Urea derivatives as tools for studying the urea-facilitated transport system.

The effects of urea structural analogues on the urea-facilitated diffusion system were examined in human red cell membranes (pink ghosts) and in antidiuretic hormone(ADH)-stimulated frog urinary bladder epithelia. In both tissues, urea permeability (P(urea)) was dramatically but reversibly inhibited by a number of urea analogues, such as 1-(3,4-dichlorophenyl)-2-thiourea (DCPTU). This urea derivative reduced the urea flux in a dose-dependent manner (90% inhibition of P(urea) at 0.5 mM concentration of DCPTU). With the aim of obtaining irreversible markers of red cell and urinary bladder urea transport systems, urea derivatives were modified by addition of an azido residue (N3) and preliminary experiments of photoaffinity labelling were carried out. Two synthetic urea derivatives: 1-(3-azido-4-chlorophenyl)-2-thiourea (ACPTU) and 1-(3-azido-4-chlorophenyl)-3-methyl-2-thiourea (Me-ACPTU) were shown to be very potent inhibitors of P(urea) when used in the absence of light, with IC50 values 60.3 microM and 31.6 microM respectively, as measured in frog urinary bladder. Both these molecules appeared to bind covalently to the urea carrier in both frog urinary bladder and human pink red cell ghosts, when illuminated in the presence of the tissue: the urea flux, which fell to 30-70% of the value obtained in the presence of ADH after inhibitor addition, remained low after the preparation had been illuminated for 30 min and the inhibitor removed. These results provide an interesting approach to the urea carrier analysis, particularly to the urea or urea analogue binding site on the transport protein.

Affinity Labels↗

PubMed2000

In vivo urea cycle flux distinguishes and correlates with phenotypic severity in disorders of the urea cycle.

Urea cycle disorders are a group of inborn errors of hepatic metabolism that result in often life-threatening hyperammonemia and hyperglutaminemia. Clinical and laboratory diagnosis of partial deficiencies during asymptomatic periods is difficult, and correlation of phenotypic severity with either genotype and/or in vitro enzyme activity is often imprecise. We hypothesized that stable isotopically determined in vivo rates of total body urea synthesis and urea cycle-specific nitrogen flux would correlate with both phenotypic severity and carrier status in patients with a variety of different enzymatic deficiencies of the urea cycle. We studied control subjects, patients, and their relatives with different enzymatic deficiencies affecting the urea cycle while consuming a low protein diet. On a separate occasion the subjects either received a higher protein intake or were treated with an alternative route medication sodium phenylacetate/benzoate (Ucephan), or oral arginine supplementation. Total urea synthesis from all nitrogen sources was determined from [(18)O]urea labeling, and the utilization of peripheral nitrogen was estimated from the relative isotopic enrichments of [(15)N]urea and [(15)N]glutamine during i.v. co-infusions of [5-(amide)(15)N]glutamine and [(18)O]urea. The ratio of the isotopic enrichments of (15)N-urea/(15)N-glutamine distinguished normal control subjects (ratio = 0.42 +/- 0.06) from urea cycle patients with late (0.17 +/- 0.03) and neonatal (0.003 +/- 0.007) presentations irrespective of enzymatic deficiency. This index of urea cycle activity also distinguished asymptomatic heterozygous carriers of argininosuccinate synthetase deficiency (0. 22 +/- 0.03), argininosuccinate lyase deficiency (0.35 +/- 0.11), and partial ornithine transcarbamylase deficiency (0.26 +/- 0.06) from normal controls. Administration of Ucephan lowered, and arginine increased, urea synthesis to the degree predicted from their respective rates of metabolism. The (15)N-urea/(15)N-glutamine ratio is a sensitive index of in vivo urea cycle activity and correlates with clinical severity. Urea synthesis is altered by alternative route medications and arginine supplementation to the degree that is to be expected from theory. This stable isotope protocol provides a sensitive tool for evaluating the efficacy of therapeutic modalities and acts as an aid to the diagnosis and management of urea cycle patients.

Adolescent↗

PubMed2002

Branchial and renal excretion of urea and urea analogues in the plainfin midshipman, Porichthys notatus.

This study investigated whether urea transport mechanisms were present in the gills of the ammoniotelic plainfin midshipman (Porichthys notatus), similar to those recently documented in its ureotelic relative (family Batrachoididae), the gulf toadfish (Opsanus beta). Midshipmen were fitted with internal urinary and caudal artery catheters for repetitive sampling of urine and blood in experiments and radiolabeled urea analogues ([(14)C]-thiourea and [(14)C]-acetamide) were used to evaluate the handling of these substances. Isosmotically balanced infusions of urea were used to raise plasma and urine urea concentrations to levels surpassing physiological levels by 8.5-fold and 6.4-fold, respectively. Despite these high urea levels, there was no observable transport maximum in either renal or branchial urea excretion rate, a result mirrored by the total uptake of fish exposed to a range of environmental urea concentrations. Permeability to urea appeared to be symmetrical in the two directions. At comparable plasma concentrations the branchial clearance rate of acetamide was 74% that of urea while branchial clearance rate of thiourea was 55% that of urea. For influx, the comparable values were 60% and 36%, indicating the same pattern. In contrast, the secretion clearance rate of acetamide by the kidney was 56% that of urea while the rate of thiourea secretion clearance was 137% greater than that of urea, with both urea and thiourea being more concentrated in the urine than in the plasma. In addition, the secretion clearance rates of thiourea and urea were significantly greater than those of water and Cl(-), whereas acetamide, water and Cl(-) were found equally in the plasma and urine, appearing to passively equilibrate between the two fluids. Based on our findings, there appear to be two distinct transport mechanisms involved in urea excretion in the plainfin midshipmen, one in the gill (a facilitated diffusion type transporter) and one in the kidney (an active transport mechanism), each of which does not saturate even at plasma urea concentrations that greatly exceed physiological levels. These transporters appear to be similar to those in the midshipman's ureotelic relative, the gulf toadfish.

Animals↗

PubMed2004

Urea may regulate urea transporter protein abundance during osmotic diuresis.

Rats with diabetes mellitus have an increase in UT-A1 urea transporter protein abundance and absolute urea excretion, but the relative amount (percentage) of urea in total urinary solute is actually decreased due to the marked glucosuria. Urea-specific signaling pathways have been identified in mIMCD3 cells and renal medulla, suggesting the possibility that changes in the percentage or concentration of urea could be a factor that regulates UT-A1 abundance. In this study, we tested the hypothesis that an increase in a urinary solute other than urea would increase UT-A1 abundance, similar to diabetes mellitus, whereas an increase in urine urea would not. In both inner medullary base and tip, UT-A1 protein abundance increased during NaCl- or glucose-induced osmotic diuresis but not during urea-induced osmotic diuresis. Next, rats undergoing NaCl or glucose diuresis were given supplemental urea to increase the percentage of urine urea to control values. UT-A1 abundance did not increase in these urea-supplemented rats compared with control rats. Additionally, both UT-A2 and UT-B protein abundances in the outer medulla increased during urea-induced osmotic diuresis but not in NaCl or glucose diuresis. We conclude that during osmotic diuresis, UT-A1 abundance increases when the percentage of urea in total urinary solute is low and UT-A2 and UT-B abundances increase when the urea concentration in the medullary interstitium is high. These findings suggest that a reduction in urine or interstitial urea results in an increase in UT-A1 protein abundance in an attempt to restore inner medullary interstitial urea and preserve urine-concentrating ability.

Animals↗

PubMed2005

Effects of intra-peritoneal injection with NH4Cl, urea, or NH4Cl+urea on nitrogen excretion and metabolism in the African lungfish Protopterus dolloi.

This study aimed to (1) determine if ammonia (as NH(4)Cl) injected intra-peritoneally into the ureogenic slender African lungfish, Protopterus dolloi, was excreted directly rather than being converted to urea; (2) examine if injected urea was retained in this lungfish, leading to decreases in liver arginine and brain tryptophan levels, as observed during aestivation on land; and (3) elucidate if increase in internal ammonia level would affect urea excretion, when ammonia and urea are injected simultaneously into the fish. Despite being ureogenic, P. dolloi rapidly excreted the excess ammonia as ammonia within the subsequent 12 h after NH(4)Cl was injected into its peritoneal cavity. Injected ammonia was not detoxified into urea through the ornithine-urea cycle, probably because it is energetically intensive to synthesize urea and because food was withheld before and during the experiment. In addition, injected ammonia was likely to stay in extracellular compartments available for direct excretion. At hour 24, only a small amount of ammonia accumulated in the muscle of these fish. In contrast, when urea was injected intra-peritoneally into P. dolloi, only a small percentage (34%) of it was excreted during the subsequent 24-h period. A significant increase in the rate of urea excretion was observed only after 16 h. At hour 24, significant quantities of urea were retained in various tissues of P. dolloi. Injection with urea led to an apparent reduction in endogenous ammonia production, a significant decrease in the hepatic arginine content, and a significantly lower level of brain tryptophan in this lungfish. All three phenomena had been observed previously in aestivating P. dolloi. Hence, it is logical to deduce that urea synthesis and accumulation could be one of the essential factors in initiating and perpetuating aestivation in this lungfish. Through the injection of NH(4)Cl + urea, it was demonstrated that an increase in urea excretion occurred in P. dolloi within the first 12 h post-injection, which was much earlier than that of fish injected with urea alone. These results suggest that urea excretion in P. dolloi is likely to be regulated by the level of internal ammonia in its body.

Amino Acids↗

PubMed2000

Urea as a marker of adequacy in hemodialysis: lesson from in vivo urea dynamics monitoring.

BACKGROUND: "Dialysis dose," a concept developed by Sargent and Gotch based on urea kinetic modeling, is a useful and recognized tool that is used to quantitate and optimize a dialysis-efficacy program. However, it has been shown that oversimplification of the "dialysis adequacy" concept to the Kt/V index might lead to dramatic underdialysis and subsequent deleterious consequences on morbidity and mortality of dialysis patients. With this perspective, the determination of Kt/V must be very cautious and rely on accurate measurement of postdialysis urea concentration and its use integrated as a tool in a quality-assurance process. METHODS: In this study, we analyzed urea dynamics by means of a blood side (ultrafiltrate) continuous online urea monitoring system interfaced with a two-pool model hosted in a microcomputer. The study was designed to provide instantaneous dialysis performances (body and dialyzer clearances, dialyzer mass transfer coefficient) and to determine the in vivo functional permeability characteristics of the patient [intercompartment urea mass transfer coefficient (Kc)]. Thirteen end-stage renal disease patients (age 54 +/- 16 years; 12 male and 1 female) were studied during nine consecutive dialysis sessions (3 weeks). RESULTS: Urea kinetics obtained from the urea monitoring system fitted closely the urea kinetic modeling prediction, confirming the validity of the double-pool model structure. Effective in vivo urea mass transfer coefficient averaged 912 +/- 235 mL/min/1.73 m2, a value close to those reported with more invasive methods. Large variations ranging from 363 to 1249 mL/min were observed among patients, confirming very large interindividual patient permeability differences. Interestingly, the urea mass transfer coefficient was inversely correlated with the postdialysis rebound values. Intraindividual variations were also noted as a function of time denoting functional changes in urea mass transfer coefficient values. The urea distribution volume was 38.1 +/- 7, 8 L (53 +/- 8% body weight). V1 referring to the extracellular volume and V2 to the intracellular volume were 9 +/- 2 L (13 +/- 2% body weight) and 29.2 +/- 6.6 L (41 +/- 1.3% body wt), respectively. The extracellular/intracellular volume ratio was 0.31 (approximately one third) and was not as usually defined by the paradigm 1/2 ratio. CONCLUSION: Online double-pool urea kinetic modeling gave a new insight in urea kinetic modeling approach. Urea dynamics fit perfectly a double-compartment model structure. Accessible extracellular volume to hemodialysis is smaller than expected. The in vivo urea mass transfer coefficient must be considered as an individual and variable characteristic of ESRD patients that should be taken into consideration when prescribing the hemodialysis schedule.

Adult↗

PubMed1981

Urea handling by the medullary collecting duct of the rat kidney during hydropenia and urea infusion.

Previous micropuncture studies of distal tubule fluid and ureteral urine have indicated a varying degree of urea reabsorption in the collecting duct. In the present experiments the microcatheterization technique was used to directly determine urea, Na, K, total solute and fluid reabsorption along the length of the medullary collecting duct in anesthetized hydropenic rats and in rats given low dose urea infusion (Purea 18.9 mM/l). In hydropenic rats, the remaining fraction of filtered urea did not change significantly along the collecting duct, as indicated both by regression analysis of all samples and by comparison of paired samples from the corticomedullary junction and papillary tip. During low dose urea infusion, urine osmolality increased in proportion to the increase in urea concentration and again there was no net urea reabsorption between the beginning and end of the duct. However, during urea infusion, analysis of samples from the beginning, mid-zone, and end of the collecting duct indicated that urea entry occurred in the proximal portion of the duct (beginning to mid-zone, P less than 0.01) and that urea reabsorption occurred in the distal portion (mid-zone to end, P less than 0.01). The lack of significant net urea reabsorption along the duct despite the excretion of moderately concentrated urine, has despite the excretion of moderately concentrated urine, has implications for the concept of medullary urea recycling and for models of the urinary concentrating mechanism. The finding of functional heterogeneity with respect to urea handling in the collecting duct in vivo, with both reabsorption are secretion being demonstrated, raises the possibility that internal recycling of urea in the medullary collecting duct itself may contribute to maintenance of a high papillary interstitial urea concentration.

Animals↗

PubMed1980

The effects of dietary sucrose and the concentration of plasma urea and rumen ammonia on the degradation of urea in the gastrointestinal tract of cattle.

1. The rates of entry of urea into plasma, of urea degradation in the gastrointestinal tract, and the partition of that degradation between the rumen and post-ruminal tract were determined by use of [14C]urea and NaH14CO3 in Hereford steers receiving hay diets with or without sucrose. The concentrations of plasma urea and rumen ammonia were varied by infusions of urea into the rumen or abomasum. 2. For all diets, plasma urea concentration was related to urea entry rate, to degradation of urea in the whole gastrointestinal tract, and to its degradation in the post-ruminal tract, but the relationship with its degradation in the rumen was poor. 3. Degradation of urea in the rumen was related in a multiple regression in a curvilinear manner in three groups of diets (pasture-hay alone, pasture-hay--lucerne (Medicago sativa) mixtures, diets with sucrose), and negatively to rumen ammonia concentration for pasture-hay diets, and diets with sucrose. 4. Ruminal clearance of urea (rate of urea degradation per plasma urea concentration) was negatively related to the rumen ammonia concentration for steers given diets with sucrose, of pasture-hay with or without urea infusions. Provision of sucrose in the diet significantly increased clearance. 5. Enhanced urea degradation in the rumen associated with dietary sucrose supplements accounted for 0.4 of additional microbial N synthesis in the rumen. 6. The partition of transfer of urea to the rumen via saliva and through the rumen wall is discussed.

Ammonia↗